Evidence map›Paper›PMID 30635041›Full record

ArticleStem cell research & therapy2019

IFNγ and TNFα synergistically induce apoptosis of mesenchymal stem/stromal cells via the induction of nitric oxide.

Xiaolei Li, Bingxue Shang, Ya-Nan Li, Yufang Shi, Changshun Shao

Open access · goldAbstract read
In one paragraph

Article in Stem cell research & therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
6.8field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

49 citing papers in PubMed, 81 citations in OpenAlex.

  1. Mesenchymal Stromal Cell-Based Cell-Drug Conjugates for the Treatment of Acute Liver Failure.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  8. NINJ1 impairs the anti-inflammatory function of hUC-MSCs with synergistic IFN-γ and TNF-α stimulation.Chinese journal of traumatology = Zhonghua chuang shang za zhi · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Xiaolei LiThe First Affiliated Hospital of Soochow University and State Key Laboratory of Radiation Medicine and Protection, Institutes for Translational Medicine, Soochow University, Suzhou, 215123, Jiangsu, China.
Bingxue ShangThe First Affiliated Hospital of Soochow University and State Key Laboratory of Radiation Medicine and Protection, Institutes for Translational Medicine, Soochow University, Suzhou, 215123, Jiangsu, China.
Ya-Nan LiThe First Affiliated Hospital of Soochow University and State Key Laboratory of Radiation Medicine and Protection, Institutes for Translational Medicine, Soochow University, Suzhou, 215123, Jiangsu, China.
Yufang ShiThe First Affiliated Hospital of Soochow University and State Key Laboratory of Radiation Medicine and Protection, Institutes for Translational Medicine, Soochow University, Suzhou, 215123, Jiangsu, China. yfshi@suda.edu.cn.
Changshun ShaoThe First Affiliated Hospital of Soochow University and State Key Laboratory of Radiation Medicine and Protection, Institutes for Translational Medicine, Soochow University, Suzhou, 215123, Jiangsu, China. shaoc@suda.edu.cn.
First Affiliated Hospital of Soochow University · CNSoochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMesenchymal stem/stromal cells (MSCs) have been widely used to treat various inflammatory diseases. The immunomodulatory capabilities of MSCs are usually licensed by inflammatory cytokines and may vary depending on the levels and the types of inflammatory cytokines. However, how the inflammatory microenvironment affects the fate of MSCs remains elusive. Here we characterized the molecular mechanism underlying the apoptosis of mouse MSCs triggered by the synergistic action of IFNγ and TNFα.

methodsWe isolated and expanded MSCs by flushing the femoral and tibial bone marrow of wild-type, iNOS

resultsIFNγ and TNFα synergistically trigger apoptosis of mouse BM-MSCs. The two cytokines were shown to stimulate the expression of inducible nitric oxide synthase (iNOS) and consequently the generation of nitric oxide (NO), which is required for the apoptosis of mouse BM-MSCs. The two cytokines similarly induced apoptosis in Fas

conclusionsIFNγ/TNFα-induced apoptosis in mouse MSCs is mediated by NO. Our findings shed new light on cytokine-induced apoptosis of MSCs and have implications in MSC-based therapy of inflammatory diseases.

Indexed as

AnimalsApoptosisAutophagyCell ProliferationCellular MicroenvironmentEndoplasmic Reticulum Stressfas ReceptorGene Expression Regulation, DevelopmentalHumansInflammationInterferon-gammaMesenchymal Stem CellsMesenchymal Stem Cell TransplantationMiceMice, KnockoutNitric OxideFas protein, mousefas ReceptorIFNG protein, mouseInterferon-gammaNitric OxideNitric Oxide Synthase Type IINos2 protein, mouseTumor Necrosis Factor-alphaApoptosisAutophagyInflammationiNOSMesenchymal stem/stromal cellsNitric oxide

Identifiers

PMID30635041
PMCPMC6330503
OpenAlexW2941919396

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.